共查询到17条相似文献,搜索用时 93 毫秒
1.
慢性HBV感染人群数量庞大,HBV不仅损害肝脏,肾脏也是主要受累器官之一,HBV相关肾小球肾炎(HBV-GN)是由HBV感染引起的继发性肾小球肾炎,是HBV感染最常见的肝外并发症之一。HBV-GN多见于儿童及中青年人,男性多见,临床上以不同程度蛋白尿为主要表现,可伴有血尿和高血压,最常见病理类型为膜性肾病,其次为系膜增生性肾小球肾炎和IgA肾病。HBV-GN起病隐匿,缺乏特征性的症状及病理学表现,易与各种肾小球肾炎混淆,导致漏诊误诊。HBV-GN发病机制复杂,涉及免疫紊乱、病毒直接损伤、遗传等诸多环节,其中免疫复合物沉积学说已得到广泛认可。近年来关于HBV-GN发病机制、诊断及治疗方面的研究取得了一些重要进展。本文将对此进行综述,希望为临床诊治提供参考。 相似文献
2.
HBV相关性肾炎的抗病毒治疗研究进展 总被引:1,自引:0,他引:1
HBV相关性肾炎(HBV-associated glomerulonephritis,HBV-GN)是HBV慢性感染最常见的肝外表现之一,主要表现为免疫复合物介导的肾小球疾病。这类患者情况特殊、病情复杂,通常须进行针对性的抗病毒治疗,故及时把握治疗时机以及正确选用抗病毒药物对HBV-GN治疗极为关键,但迄今为止仍无规范统一的治疗策略。本综述参考国内外最新信息,对HBV-GN的抗病毒治疗研究进展以及各抗病毒药物的疗效、安全性等进行总结,以期为临床决策提供参考。 相似文献
3.
正1病例资料患者男性,27岁,于2005年诊断为"乙型肝炎",未规范治疗,入院前2周门诊查肝功能:TBil 34.6μmol/L,DBil16.11μmol/L,ALT 91 U/L,AST 191 U/L,白蛋白(Alb)33.4g/L;血清HBV DNA载量:4.65×10~4IU/ml;腹部B超提示"肝 相似文献
4.
HBV相关性肾炎的抗病毒治疗 总被引:1,自引:0,他引:1
乙型肝炎病毒相关性肾炎(hepatitis B virus associated glomerulonephritis,HBV-GN)是HBV感染的表现之一.已有多种药物被用于治疗HBV-GN,但迄今为止尚无最佳的治疗方案.抗病毒(包括干扰素和核苷类似物)治疗HBV-GN能有效抑制HBV复制、缓解蛋白尿,且HBeAg的... 相似文献
5.
丙型肝炎病毒感染与肾小球肾炎 总被引:3,自引:0,他引:3
自1989年首次分离出丙型肝炎RNA病毒以来,人们也重视丙型肝炎病毒与肾脏疾病的关系。我们首先采用酶联免疫法检测570例经肾活检证实肾小球肾炎患者血清及100例健康献血员血清的抗丙型肝炎病毒抗体(抗HCV).又用聚合酶链反应(PCR)法对血清抗HCV阳性患者进行了血清HCV一RNA检测。肾炎患者血清的抗HCV阳性者为34例(6%);抗HCV与乙型肝炎表面阳性标志物同时存在者为2例。抗HCV阳性在各型肾小球病理损伤中的阳性例数与正常对照及其余病理损伤组比较,差异有显著性(P<0.05);而抗体阳性34例中HCV一RNA阳性者21例,亦广泛分布于各型肾小球疾病中。抗HCV阳性的34例患者均以蛋白尿为主要表现,血肌酐增高者9例,ALT增高者6例,血清补体C_3降低者4例。本资料表明HCV感染伴随之肾脏病理改变不均一,似以新月体肾炎、微小病变肾病、局灶节段性肾小球硬化病理类型HCV感染的可能性更大。提示HCV感染与某种肾小球疾病之间无肯定的致病关系(包括膜增生性肾炎),似以2种疾病同时并存的可能性大。 相似文献
6.
目的: 探讨乙型肝炎病毒相关性肾炎(HBVGN)易感性与HBV基因变异的关系.方法: 选取HBV-GN患者19例为试验组, 慢性HBV感染者22例为对照组, 应用基因测序技术检测HBV血清C基因区、CP区基因位点的变异.结果: CP区中nt1727和nt1773位点试验组的变异率显著高于对照组(100% vs 50.0%, 47.4%vs 13.6%, 均P <0.05). nt1762/1764联合变异率在2组中的差别无统计学意义(P >0.05). C基因区中nt2011变异率试验组显著低于对照组(10.5% vs 40.9%, P <0.05). nt2005、nt2201、nt2245和nt2290变异率在2组中的差别无统计学意义(P >0.05).结论: HBV-GN易感性可能与HBV的基因变异有关. 相似文献
7.
原纤维性肾小球肾炎是一组新的肾小球疾病。本文从临床情况、光镜检查、电镜检查以及免疫荧光检查等方面作一综合介绍。 相似文献
8.
9.
乙肝相关性肾小球肾炎(hepatitis B virus associated glomerulonephritis,HBV-GU)是指由乙肝病毒所致肾功能损害,是临床上常见的继发性肾脏病。其发病机制不明、起病隐匿、无特征性症状及肾脏病理学表现,易与各型肾小球肾炎相混淆,且治疗上对是否应用激素长期存在争议。 相似文献
10.
本文介绍了肾小球肾炎肺出血综合征发病机理、流行病学和临床表现、化验检查、自然病程和预后、诊断及治疗方法的近年研究进展。 相似文献
11.
核苷(酸)类似物抗病毒治疗乙型肝炎病毒相关性肾炎疗效观察 总被引:2,自引:0,他引:2
目的评价核苷(酸)类似物治疗乙型肝炎(乙肝)病毒相关性。肾炎(hepatitis B virus—associated glomerulonephritis,HBV—GN)合并慢性乙肝或肝硬化的临床疗效和安全性。方法选择病理诊断为HBV—GN,同时合并慢性乙肝或肝硬化的患者共36例。患者分成2组:核苷(酸)类似物抗病毒治疗组25例,给予拉米夫定0.1g,1次/d,或恩替卡韦0.5mg,1次,d,空腹口服;对照组11例,未给予核苷(酸)类似物抗病毒治疗。2组均给予常规保肝降酶及保护肾功能的治疗。观察治疗前后临床指标变化,包括用药期间尿蛋白排泄情况、肝。肾功能和乙肝病毒学指标以及不良反应。结果治疗12个月时,抗病毒治疗组24h尿蛋白定量较治疗前明显减少,血清ALB较治疗前明显升高;对照组24h尿蛋白定量和ALB与治疗前相比无显著改善。2组ALT和AST水平治疗后均明显改善,但抗病毒治疗组ALT和AST下降幅度明显大于对照组。抗病毒治疗组血清HBVDNA水平治疗后明显下降,对照组治疗前后无明显变化。抗病毒治疗组治疗12个月时的完全缓解率、总有效率明显高于对照组。结论核苷(酸)类似物治疗HBV—GN,可显著降低尿蛋白,使ALB升高,HBVDNA水平降低,缓解肾病综合征的临床症状,取得满意疗效,且耐受性好,未见明显不良反应。 相似文献
12.
Yu Zhang Jian-Hua Zhou Xiao-Ling Yin Feng-Yu Wang 《World journal of gastroenterology : WJG》2010,16(6):770-777
AIM:To evaluate the efficacy of antiviral or corticosteroid treatment on hepatitis B virus-associated glomerulonephritis(HBV-GN) . METHODS:Six and five trials were used respectively to evaluate the efficacy of either antiviral or corticosteroid treatment on HBV-GN.Pediatric patients were pooled separately to assess their response to the above treatment modalities.The primary and secondary outcomes were remission of proteinuria and clearance of Hepatitis B e-antigen(HBeAg) ,respectively.A fixed or random eff... 相似文献
13.
乙型肝炎(乙肝)相关性肾炎作为最常见的并发症之一常见于慢性乙肝病毒感染患者。虽部分乙肝相关性肾炎患者可自行缓解,并维持肾功能正常,但仍有部分患者发展为肾功能不全,最终进入透析阶段,故进一步研究其有效治疗方法甚为重要。目前已有多种药物用于治疗乙肝相关性肾炎,如激素、干扰素、拉米夫定等,但对于确切疗效仍有争议。现将乙肝相关性肾炎发病机制及治疗的研究进展作一总结。 相似文献
14.
拉米夫定联合中药肝肾饮治疗乙型肝炎病毒相关性肾炎的研究 总被引:1,自引:0,他引:1
目的:观察拉米夫定结合中药肝肾饮治疗临床表现为肾炎综合征的乙型肝炎病毒相关性肾炎(HBV-GN)的疗效。方法:18例符合条件的HBV-GN患者,随机分成治疗组和对照组,对照组口服拉米夫定100mg/d,治疗组在对照组基础上加用中药肝肾饮,治疗12个月,随访6个月。结果:两组患者治疗后24小时与治疗前比较尿蛋白定量、血清白蛋白及肾功能的差异有统计学意义,治疗组和对照组在治疗后24小时尿蛋白定量、肾功能比较,差异有统计学意义。两组中1例患者因使用拉米夫定出现YMDD变异,1例患者因使用拉米夫定出现头痛。结论:拉米夫定结合中药肝肾饮治疗乙型肝炎病毒相关性肾炎安全有效,且较单纯应用拉米夫定的对照组疗效为佳。 相似文献
15.
16.
HBsAg-negative hepatitis B virus infections in hepatitis C virus-associated hepatocellular carcinoma
This study was conducted to evaluate reports that hepatitis B virus (HBV) DNA sequences can be found in the serum and/or tumour tissue from some hepatocellular carcinoma (HCC) patients who have no detectable hepatitis B surface antigen (HBsAg) in their sera. Such HBV infections would be highly atypical, because prospective studies have shown a clear succession of specific serologic markers during and after most HBV infections. As most HBsAg-negative HCC patients in Japan have hepatitis C virus (HCV) infections, the present study was conducted to determine whether some of these patients actually have unrecognized HBV infections. Thirty newly diagnosed HCC patients from Kurume, Japan, with antibody to the hepatitis C virus (anti-HCV) were studied. None of the 30 had HBsAg detectable in their serum. Of 22 for whom test results for antibodies to the hepatitis B core antigen (anti-HBc) and antibodies to HBsAg (anti-HBs) were available, 14 (64%) had anti-HBc and anti-HBs, four (18%) had anti-HBc alone, and four (18%) had no HBV markers. Nested polymerase chain reaction was used to detect the HBV surface (S), core (C), polymerase (P) and core promoter gene sequences in the HCC tissues and in the adjacent nontumorous liver tissues. HBV DNA was detected in HCC and/or adjacent nontumorous liver in 22 of 30 (73%) patients [detected in both HCC and nontumorous liver in 19/30 patients (63%)]. Among the 22 patients with detectable HBV DNA, more than one HBV gene was detected in 10 (46%). Among the four patients whose sera were negative for all HBV markers, three had HBV DNA in either HCC and nontumorous liver (two cases) or only in the nontumorous liver (one case); HBV DNA could not be detected in tissues from the fourth patient. In 18 of 21 (86%) patients with detectable HBV core promoter sequences, mutations at both nucleotides 1762 (A-GT) and 1764 (G-A) in the core promoter region were found. No deletions were detected in the core promoter gene region of the type reported to be associated with some cases of HBsAg-negative HBV infection. Thus, HBV DNA was detectable in 22 (73%) HBsAg-negative, anti-HCV-positive HCCs, including three (10%) who were also negative for anti-HBc and anti-HBs. HBV mutations at both nucleotides 1762 (A-GT) and 1764 (G-A) in the core promoter region were found in the majority of cases, mutations that have previously been reported in HBV that is integrated in HCC DNA. In serologic surveys to determine etiologic associations of HCC, patients such as those in this study would have been incorrectly designated as having 'HCV-associated HCC,' whereas the data in this study suggest that HBV could have played a role in the development of their HCCs. 相似文献